Abstract
There have been few studies investigating interactions of G-protein beta3 subunit (GNB3) C825T (rs5443) and dietary sodium intake on the risk of hypertension, i.e., BP salt sensitivity. The study aims to evaluate joint effects of GNB3 polymorphisms and sodium consumption on the development of hypertension. A cohort-based case-control study was conducted in 2014. There are 233 participants with newly diagnosed hypertension in the case group and 699 participants in the gender-matched control group. The primary outcome is the development of hypertension over a 10-year period. The determinants of hypertension were three genotypes of SNP in GNB3 (TT; CT; and CC) and two dietary salt categories on the basis of the level of sodium consumption representing high (>4800 mg/day) and low-sodium (<2400 mg/day) diets. The development of hypertension increased with participants carrying TT genotype and high-sodium diets comparing with those carrying TC or CC genotype with low-sodium diets (adjusted OR 3.23, 95% CI 1.52–6.83) (Rothman synergy index = 3.79). The study suggests that GNB3 C825T polymorphism may influence the response of the renin-angiotensin system to high-sodium diet. It implies that GNB3 can be served as an easy, inexpensive, and early genetic marker of salt sensitivity to blood pressure. Salt-sensitive individuals should pay more attention to salt intake to reduce cardiovascular morbidity or mortality.
Highlights
Hypertension remains a major risk factor of cardiovascular disease morbidity and mortality.It has been recognized that both genetic and environmental factors play key roles in the causes of hypertension, as well as their interactions [1]
A cohort-based case-control study provided a suitable method to evaluate the role of dietary sodium intake in the development of hypertension
The correlation between daily dietary sodium intake and mean of two 24-h urinary collections for sodium was 0.75
Summary
Hypertension remains a major risk factor of cardiovascular disease morbidity and mortality. It has been recognized that both genetic and environmental factors play key roles in the causes of hypertension, as well as their interactions [1]. It is important to have a better understanding of environmental, dietary, and behavioral factors. Identifying determinants of genetic susceptibility to those factors would be beneficial. Several genes known or suspected to be involved in blood pressure (BP) pathways—such as renin-angiotensin system, neuroendocrine system, vasoactive peptides, nitric oxide, calcium and potassium channels, wnt/beta-catenin signaling pathways, kidney solute transport and kidney structure or proteins—have been identified in genome-wide association studies in the general population [2]. Intracellular signal transduction was considered as one of the most important pathways, Int. J. Public Health 2018, 15, 1110; doi:10.3390/ijerph15061110 www.mdpi.com/journal/ijerph
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